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In this experiment, a series of poly(propylene 2,5-furan dicarboxylate)-b-poly(ethylene glycol) (PPFEG) copolymers with different ratios were synthesized using melt polycondensation of dimethylfuran-2,5-dicarboxylate (DMFD), 1,3-propanediol (PDO) and poly(ethylene glycol) (PEG). The effect of PEG content on the crystallization behavior of the poly(propylene 2,5-furan dicarboxylate) (PPF) copolymers was investigated. For PPF, the nucleation density of the β-crystals was higher than that of α-crystals. As Tc increases, the β crystals are suppressed more, but at Tc = 140 °C, the bulk of PPF has already been converted to α crystals, which crystallize faster at higher nucleation densities, resulting in a difference in polymer properties. For this case, we chose to add a soft segment material, PEG, which led to an early multi–melt crystallization behavior of the PPF. The addition of PEG led to a decrease in the crystallization temperature of PPF, as well as a decrease in the cold crystallization peak of PPF. From the crystalline morphology, it can be seen that the addition of PEG caused the transformation of the PPF crystalline form to occur earlier. From the crystalline morphology of PPF at 155 °C, it can be observed that the ring-banded spherical crystals of the PPF appear slowly with increasing time. With the addition of PEG, spherical crystals of the ring band appeared earlier, and even appeared first, and then disappeared slowly.

Objective To investigate the hepatoprotective effect and anti-hepatocyte pyroptosis effect of Yinchenhao decoction synergized with umbilical cord mesenchymal stem cells (UcMSCs) in vitro and vivo models of acute liver failure (ALF), as compared to single-drug treatment. Methods UcMSCs were extracted from umbilical cords and identified using electron microscopy and flow cytometry. Then the exosomes released from ucMSCs (UcMSCs-exo) were isolated through ultracentrifugation, and ucMSCs-exo were identified by nanoparticle tracking analysis (NTA), transmission electron microscopy, and Western blot for CD63 and CD9. Human hepatocyte cell line LO2 cells were stimulated by 100 ng/mL lipopolysaccharide (LPS) and 5 mmol/L adenosine triphosphate (ATP) to construct a vitro model of ALF. The cells were randomly divided into the following groups: a normal control group, a model group, a Yinchenhao decoction treatment group, a ucMSCs-exo treatment group, and a combination treatment group. The morphological changes of LO2 were observed under the electron microscope, the mortality of LO2 cells was detected by flow analysis, the expression of pyroptosis-related proteins Caspase-1 and Cleaved-Caspase-1 was detected by Western blot, and the expression of pyroptosis-related cytokines IL-1β and IL-18 was detected by ELISA. Then, fifty 6-8-week-old male C57BL/6 mice were randomly divided into the following groups: normal control group, model group, Yinchenhao decoction treatment group, ucMSCs-exo treatment group, and combined treat- ment group. Each group consisted of 10 mice. The ALF mouse model was constructed by intraperitoneal injection of 10 μg/kg LPS and 800 mg/kg D-galactosamine (D-GalN). After successful modeling, each group was given the appropriate drug interventions, and the ucMSCs-exo and combined treatment groups were injected with ucMSCs-exo interventions in the tail vein, and the drugs were administered continuously for 3 days. After 12 hours of intervention, serum specimens and liver tissues were collected from each group. The expression levels of ALT and AST were detected, and the liver tissues were stained with HE to observe the pathological changes. Results In the ALF cell model, hepatic cell death was inhibited in the Yinchenhao decoction treatment group, the ucMSCs-exo treatment group, and the combination group (P < 0.05). The rate of hepatic cell death in the combination treatment group was significantly reduced (P < 0.05). Initially, the study aimed to explore the effect on hepatic cell pyroptosis, and it was found that the combination treatment group could effectively suppress hepatocellular cell death more effectively compared to the single treatment groups. The combined treatment group significantly reduced the expression of the pyroptosis-related protein Cleaved-Caspase-1, as well as the cytokines IL-1β and IL-18 (P < 0.05). However, there was no statistically significant difference in the expression of Caspase-1 (P > 0.05). In the vivo model, the single Yinchenhao decoction treatment group, the ucMSCs-exo treatment group, and the combined treatment group were able to effectively reduce the serum ALT and AST levels compared to the model group(P < 0.05). Additionally, these treatments were found to attenuate hepatocellular necrosis and the infiltration of inflammatory cells. Compared to the group treated with only Yinchenhao decoction or only ucMSCs-Exo, the group that received combined treat- ment showed a greater decrease in serum ALT and AST levels. Additionally, there was a reduction in the infiltration of inflammatory cells and the extent of cell death in the liver tissues (P < 0.05). Conclusions The combination of Yinchenhao decoction and ucMSCs-exo demonstrated a significantly better hepatoprotective effect in the ALF vivo model compared to the individual treatments of Yinchenhao decoction or ucMSCs-exo alone. Furthermore, this combination treatment was able to effectively inhibit hepatocyte pyroptosis. [ABSTRACT FROM AUTHOR]

Background: Radiofrequency ablation (RFA) is an effective therapy for hepatocellular carcinoma (HCC). However, incomplete radiofrequency ablation (IRFA) can promote the progression of residual cancer cells, which is a serious problem in the clinical application of RFA. Therefore, it is of great significance to explore the mechanism and countermeasures of the progression of residual tumors after IRFA. Our previous study confirmed that IRFA can activate the hypoxia/ autophagy pathway of residual tumors in mice and then induce the proliferation of residual tumor cells. Additionally, we found a metal ruthenium complex [Ru(bpy)2(ipad)](ClO4)2 (Ru, where bpy = 2,2'-bipyridine and ipad = 2-(anthracene-9,10-dione-2-yl)imidazo[4,5-f][1,10]phenanthroline) can effectively inhibit hypoxia-inducible factor (HIF-1α) and has good anti-tumor effect in a hypoxic environment; however, whether Ru could suppress the proliferation of residual tumor cells after IRFA is unknown., Objective: This study intends to evaluate the effect of Ru in suppressing the proliferation of residual hepatocellular carcinoma after IRFA in a mice model., Methods: The Hepa1-6 xenograft mouse model was established in C57BL/6 mice to simulate clinical IRFA. H&E staining was used to evaluate the biosafety of major organs in the treated mice. TUNEL assay was employed to assess the antitumor effect. Immunohistochemically and immunofluorescence staining was performed to detect the expression of HIF-1α and autophagy-related proteins. The ELISA assay was used to examine the cytokines of interferon-gamma (IFN-γ) and interleukin 10 (IL-10)., Results: Our findings revealed that the residual tumor relapsed via the HIF-1α/LC3B/P62 autophagy- related pathway after IRFA, while Ru could suppress this process. In addition, it was demonstrated that Ru could effectively activate the immune system of the mice and reverse the tumor immune suppression microenvironment after IRFA., Conclusion: The ruthenium complex Ru could suppress the proliferation of residual hepatocellular carcinoma cells after IRFA in the mice model. This study introduces a novel approach that combines the use of ruthenium complexes with IRFA, offering a potential solution to address the reoccurrence of residual liver cancer following IRFA in clinical settings., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Acute liver failure (ALF) is a severe liver disease caused by disruptions in the body's immune microenvironment. In the early stages of ALF, Kupffer cells (KCs) become depleted and recruit monocytes derived from the bone marrow or abdomen to replace the depleted macrophages entering the liver. These monocytes differentiate into mature macrophages, which are activated in the immune microenvironment of the liver and polarized to perform various functions. Macrophage polarization can occur in two directions: pro-inflammatory M1 macrophages and anti-inflammatory M2 macrophages. Controlling the ratio and direction of M1 and M2 in ALF can help reduce liver injury. However, the liver damage caused by pyroptosis should not be underestimated, as it is a caspase-dependent form of cell death. Inhibiting pyroptosis has been shown to effectively reduce liver damage induced by ALF. Furthermore, macrophage polarization and pyroptosis share common binding sites, signaling pathways, and outcomes. In the review, we describe the role of macrophage polarization and pyroptosis in the pathogenesis of ALF. Additionally, we preliminarily explore the relationship between macrophage polarization and pyroptosis, as well as their effects on ALF., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Xie and Ouyang.)

Xpert Xpress Flu/RSV is a fast and automated real-time nucleic acid amplification tool for detecting influenza virus and respiratory syncytial virus (RSV). The aim of this study was to verify the accuracy of Xpert Xpress Flu/RSV for detecting influenza virus and RSV. PubMed, EMBASE, Cochrane Library, and Web of Science databases were searched up to October 2020. The quality of the original research was assessed using the Quality Assessment of Diagnostic Accuracy Studies-2 guidelines. Meta-DiSc 1.4 software was used to analyze the sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, diagnostic odds ratio, and summary receiver operating characteristic curve. Deek's funnel plot asymmetry test was used to evaluate the publication bias using the Stata 12.0 software. Ten studies with 25 fourfold tables were included in the analysis. The sensitivity of Xpert Xpress Flu/RSV for detecting influenza A, influenza B, and RSV were 0.97, 0.98, and 0.96, respectively, and the specificities were 0.97, 1.00, and 1.00, respectively. Compared with other common clinical real-time reverse transcription-polymerase chain reaction (RT-PCR), Xpert Xpress Flu/RSV is a valuable tool for diagnosing influenza virus and RSV with high sensitivity and specificity.

Background: To date, studies have shown inconsistent results of treatment with bone marrow-derived stem cells (BMDSC) for patients with liver cirrhosis. This study aims to compare the efficacy and safety of BMDSC and standard therapy for liver cirrhosis., Methods: Articles from PubMed, Embase, and the Cochrane library were searched from inception to April 2018. The index included Model for End-stage Liver Disease (MELD), alanine aminotransferase (ALT), albumin, total bilirubin (TBIL), prothrombin time (PT), Child-Pugh score, and all-cause mortality., Results: A total of 9 studies with a total of 424 patients with liver cirrhosis were included in final meta-analysis. BMDSC therapy was associated with lower MELD within 3 months (P = .010), while it had no significant impact on MELD after 6 months (P = .074). There were no differences between BMDSC and standard therapy for ALT within 3 months (P = .336) and after 6 months (P = .379). BMDSC did not affect albumin level within 3 months (P = .196) and after 6 months (P = .840). BMDSC reduced the TBIL level within 3 months (P = .037) and was not associated with the TBIL level after 6 months (P = .914). There were no differences between BMDSC and standard therapy for PT within 3 months (P = .167) and after 6 months (P = .484). The Child-Pugh scores within 3 months (P = .342) and after 6 months (P = .133) were not associated with BMDSC treatment for liver cirrhosis patients. Finally, the BMDSC was not associated with the risk of all-cause mortality, as compared with standard therapy (P = .622)., Conclusions: BMDSC treatment for patients with liver cirrhosis could improve short-term MELD and TBIL, but not the risk of mortality, as compared with standard therapy.